ArticleNature cell biology2025
Functional screen identifies RBM42 as a mediator of oncogenic mRNA translation specificity.
Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Ribo-Tweezer: Rapid removal of ribosomal proteins reveals additional layers of post-transcriptional gene regulation.Molecular cell · 2026Article
- Rapid Optimization Enabled by Single-Molecule Tracking: Discovery of a Potent RUVBL1/2 Inhibitor to Evaluate the Targeting of MYC-Driven Cancers.Journal of medicinal chemistry · 2026Article
- Interplay between RNA-protein interactions and RNA structures in gene regulation.FEBS open bio · 2026Review
- Photosensitive composite nanoparticles adsorbing p-shDrug delivery · 2025Article
- Discovery of Small Molecules That Inhibit MYC mRNA Translation Through hnRNPK and Induction of Stress Granule-Mediated mRNA Relocalization.International journal of molecular sciences · 2025Article
- Regulating MYC translation in cancer.Nature cell biology · 2025Article
- Exploration of RNA-binding proteins identified RPS27 as a potential regulator associated with Kaposi's sarcoma development.BMC cancer · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
Oncogenic protein dosage is tightly regulated to enable cancer formation but how this is regulated by translational control remains unknown. The Myc oncogene is a paradigm of an exquisitely regulated oncogene and a driver of pancreatic ductal adenocarcinoma (PDAC). Here we use a CRISPR interference screen in PDAC cells to identify activators of selective MYC translation. The top hit, the RNA-binding protein RBM42, is highly expressed in PDAC and predicts poor survival. We show that RBM42 binds and selectively regulates the translation of MYC and a precise suite of pro-oncogenic transcripts, including JUN and EGFR. Mechanistically, we find that RBM42 binds and remodels the MYC 5' untranslated region structure, facilitating the formation of the translation pre-initiation complex. Importantly, RBM42 is necessary for PDAC tumorigenesis in a Myc-dependent manner in vivo. This work transforms the understanding of the translational code in cancer and illuminates therapeutic openings to target the expression of oncogenes.
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